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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 8  |  Issue : 1  |  Page : 20-25

Clinicohistopathologic study of lichenoid interface dermatitis


1 Department of Pathology, Kempegowda Institute of Medical Sciences, Bengaluru, Karnataka, India
2 Department of Dermatology, Kempegowda Institute of Medical Sciences, Bengaluru, Karnataka, India

Date of Submission26-Jan-2020
Date of Decision14-Feb-2020
Date of Acceptance16-Feb-2020
Date of Web Publication20-Jun-2020

Correspondence Address:
Dr. Aparna Muralidhar
No. 137, 5th Main, Padmanabhanagar, Bengaluru - 560 070, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/amhs.amhs_11_20

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  Abstract 


Background: Interface dermatitis (IFD)/lichenoid tissue reactions are among the most frequently presenting disorders in dermatology, which in common have a constellation of histopathological features but varied clinical presentation. Aim: Clinicopathologic correlation and determination of histomorphologic changes associated with various lichenoid IFD of the skin. Materials and Methods: This was a prospective study with purposive sampling of patients reporting to the outpatient department of dermatology, venerology, and leprosy of our hospital from January 2017 to July 2018. Skin biopsies of 150 patients of either sex diagnosed provisionally as one of the lichenoid IFD on clinical grounds were studied. Clinicohistopathologic correlation was done. Results: We encountered 58 cases of classic lichen planus, seven variants of lichen planus (hypertrophic lichen planus, ashy dermatosis, lichen planus pigmentosus, actinic lichen planus, lichen planopilaris, lichen nitidus, and lichen striatus), and 16 cases of lichenoid eruptions. About 82.6% of the cases were concordant histopathologically. The peak incidence was in 20–40 years of age with an equal predilection for males and females. A majority of the lesions were multiple, pruritic, papules, and plaques involving the limbs. Histopathologically, the most consistent findings were basal cell vacuolar degeneration followed by melanin incontinence. Conclusion: Lichenoid IFDs are exclusive clinicopathological entities with several variants. Subtle features noted on histopathology help in differentiating these lesions. Understanding and interpreting these subtle changes aids in better clinical management of the patient.

Keywords: Lichen nitidus, lichen planus, lichenoid eruptions


How to cite this article:
Muralidhar A, Venugopal SB, Nandini A S. Clinicohistopathologic study of lichenoid interface dermatitis. Arch Med Health Sci 2020;8:20-5

How to cite this URL:
Muralidhar A, Venugopal SB, Nandini A S. Clinicohistopathologic study of lichenoid interface dermatitis. Arch Med Health Sci [serial online] 2020 [cited 2020 Oct 1];8:20-5. Available from: http://www.amhsjournal.org/text.asp?2020/8/1/20/287343




  Introduction Top


In 1973, Pinkus defined lichenoid tissue reactions (LTRs) as “A number of clinically diverse, poorly understood and relatively uncommon inflammatory skin diseases linked together by the presence of a pattern of common histopathological elements.”[1] This histologic pattern was referred to as interface dermatitis (IFD) by more modern workers.[2],[3],[4]

LTRs are among the most frequently presenting disorders in dermatology with varied clinical presentations. Some are common in children, while others more often affect the adult population.

IFD can be divided into two broad categories:

  • Lichenoid (cell rich) – prototype being lichen planus
  • Vacuolar (cell poor) – prototype of which is erythema multiforme.


Basal cell damage leading to cell death and/or vacuolar changes (liquefactive degeneration) is a common denominator of these disorders. Cell-mediated cytotoxicity is considered a major mechanism of pathogenesis of lichen planus, as evidenced by T-cells being the predominant cells in the inflammatory infiltrate.[5] Various factors such as mechanical trauma, systemic drugs, contact sensitivity, and infective agents including some viruses may precipitate the cell-mediated reaction.[6]

The primary morphologic changes include basal cell damage, apoptotic/necrotic keratinocytes, and an inflammatory infiltrate obscuring the dermoepidermal junction. The papillary dermis shows melanin incontinence and melanophages subsequent to basal cell damage. Long-standing cases may show fibrosis or sclerosis of the dermis. Some lesions show morphologic changes involving the adnexal structures.

Different diseases within this spectrum show variable findings depending on the disease, time of biopsy in the course of evolution, and the site of the biopsy. This study was conducted to determine the histomorphologic changes associated with various lichenoid interface dermatoses, their age, and sex distribution and clinicopathologic correlation.


  Materials and Methods Top


We undertook a 1½ years prospective study of patients with a clinical differential diagnosis of one of the lichenoid IFDs reporting to the outpatient department of dermatology in our hospital from January 2017 to July 2018. Autolyzed and inadequate biopsy specimens were excluded from the study. The study was approved by the ethical committee of our institute. Purposive sampling was done. The representative skin punch biopsies received in 10% formalin were processed. Five microns-thick sections were taken and stained with hematoxylin and eosin. Slides were evaluated and categorised into different types of lichenoid IFDs. Data collected were analyzed using frequency distribution and presented in the form of tables and charts.


  Results Top


We studied 150 cases of either sex with clinical differential diagnosis as one of the lichenoid IFDs. Of these, 58 were classic lichen planus, 76 were variants of lichen planus, and 16 were lichenoid eruptions, as seen in the [Pie Chart 1].



One hundred and twenty four (82.66%) cases were concordant on histopathology. These were ashy dermatosis, lichen planopilaris, lichen nitidus, lichen striatus, actinic lichen planus, and lichenoid eruption. Discordance was seen in 16 (27.6%) cases of classic lichen planus, five (11.6%) cases of lichen planus pigmentosus, and five (38.5%) cases of hypertrophic lichen planus, amounting to a total of 26 cases.

A majority of the patients were in the age group of 21–40 years (41.9%) with an equal predilection for males and females. Actinic lichen planus and lichenoid eruptions were more common beyond 40 years of age. Most of the patients presented within 6 months of the onset of symptoms. Patients with hypertrophic lichen planus had a longer duration of symptoms (>2 years).

Multiple lesions involving the limbs were observed in 54% of the cases [Figure 1]a and [Figure 1]b. This was followed by the face and neck (mainly the lesions of lichen planus pigmentosus and ashy dermatosis), as seen in [Figure 1]c. Genital lesions were seen in two cases of lichen planus. Three cases of lichen planopilaris presented with scalp involvement [Figure 1]d.
Figure 1: Clinical photographs of Lichenoid IFD. (a and b) Limb involvement. (c) Lichen planus pigmentosus involving face. (d) Lichen planopilaris involving scalp

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Overall, maximum number of the patients presented with pruritic papules and plaques. Lesions of lichen planus pigmentosus and ashy dermatosis were mainly macules, papules, and patches. Sun exposure was a significant history in lichen planus pigmentosus (55.26% cases), ashy dermatosis (50% cases), and actinic lichen planus (66.6% cases). Half of the cases of lichen planopilaris presented with alopecia.

As shown in [Table 1], hyperkeratosis was present in 80.6% of the cases. About 12.9% of the cases showed parakeratosis, a feature observed in lichen striatus, 50% of the cases showed lichenoid eruptions and lichen planopilaris, and few cases showed hypertrophic lichen planus, actinic lichen planus, and lichen nitidus. Epidermal thinning was observed in 50% of the cases of lichen planus pigmentosus and 75% of the cases of ashy dermatosis.
Table 1: Histologic changes

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Seventy cases exhibited acanthosis. Three cases of lichen planus and four cases of lichenoid eruption showed saw-toothing of rete ridges. Hypergranulosis was seen in 42.86% of the cases of classic lichen planus, 75% of the cases showed hypertrophic lichen planus, one case showed actinic lichen planus, and two cases showed lichenoid eruptions. Five cases each of classic lichen planus and lichenoid eruptions showed spongiosis.

Basal cell vacuolar degeneration was the most consistent finding accounting for 95.2%. Civatte bodies were found in 41.93% of the cases, predominantly in classic and hypertrophic variants of lichen planus, and in 50% of the cases of lichenoid eruptions.

Melanin incontinence resulting from basal cell damage was the most significant dermal feature (90.32% cases). Caspary Joseph spaces were found in four cases of classic lichen planus and one case each of hypertrophic lichen planus and lichen nitidus. All cases of lichen nitidus showed expanded dermal papillae with mononuclear inflammatory cell infiltrate.

Fifty eight percent cases showed band-like inflammatory infiltrate at the dermoepidermal junction. All cases had lymphocytes with admixed histiocytes in 61.3% of the cases. Lichenoid eruptions showed few eosinophils and mast cells as well.

Microscopic images are shown in [Figure 2], [Figure 3], [Figure 4], [Figure 5].
Figure 2: (a) Photomicrograph of classic lichen planus, (H and E, ×100). Inset – civatte bodies, shown by arrows, (H and E, ×400). (b) Photomicrograph of hypertrophic lichen planus, (H and E, ×100). Inset – inflammation at the tip of rete ridge, (H and E, ×400)

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Figure 3: (a) Photomicrograph of lichen planus pigmentosus, (H and E, ×100). Inset – (H and E, ×400). (b) Photomicrograph of lichen planopilaris showing perifollicular inflammation, (H and E, ×100)

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Figure 4: (a) Photomicrograph of lichen nitidus, (H and E, ×100). (b) Photomicrograph of lichen striatus, (H and E, ×100)

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Figure 5: Photomicrograph of lichenoid eruption, (H and E, ×100). Inset – eosinophils in the infiltrate, (H and E, ×400)

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  Discussion Top


IFD embraces several dermatoses under its ever-expanding domain. The cardinal features include epidermal basal layer injury and dermal mononuclear inflammatory infiltrate. Shiohara and Kano, Shiohara and Mizukawa.[7],[8] stated that the primary pathological event in LTR/IFD is an autoimmune attack by T-cells on the epidermis. In some disorders, the antigen being targeted by activated T-cells is known, as seen with alloantigens in graft versus host skin disease, Ro/SSA and La/SSB in neonatal lupus erythematosus (LE) and subacute cutaneous LE (SCLE). However, in most LTRs/IFDs, the targeted antigen is unknown, with cross-reactivity between environmental antigens (for example – viral, drug, and chemical) and self-antigens being suspected.[9]

IFD can be a manifestation of systemic diseases such as LE, graft versus host disease, Steven–Johnson syndrome, and toxic epidermal necrolysis. The skin lesions of chronic graft versus host disease may resemble lichenoid reactions clinically. However, the inflammation tends to be more perivascular instead of band like.[10] Different clinical subtypes of LE may present with variable features of IFD. Discoid LE shows characteristically a superficial and deep periadnexal dermal inflammatory infiltrate, especially around the pilosebaceous units. The reaction pattern is mainly vacuolar. Systemic Lupus Erythematosus (SLE) typically shows thickened basement membrane and dermal mucin.[11]

Paraneoplastic pemphigus is a multisystem autoimmune disease with polymorphous skin lesions. It has several clinical variants, one of which is lichen planus like. Few associated internal malignancies include Hodgkin's and non-Hodgkin's lymphoma, thymoma, hepatocellular, and uterine carcinomas.[11] It should be considered as a differential diagnosis after ruling out other common causes of the presenting skin lesions with appropriate history and workup. Paraneoplastic pemphigus is resistant to most therapies. Initial treatment is aimed at the underlying malignancy to reduce the burden of autoantibodies.[11]

Idiopathic lichen planus has been associated with diseases of altered immunity such as ulcerative colitis, vitiligo, dermatomyositis, primary biliary cirrhosis, and primary sclerosing cholangitis.[12]

A study examining the patterns of expression of intercellular adhesion molecule 1 (ICAM 1) showed that keratinocytes in the normal epidermis have a low constitutive expression of ICAM 1, thereby rendering them resistant to interaction with leukocytes. In lichen planus, ICAM 1 is expressed in the basal keratinocytes. In contrast, there is a diffuse epidermal expression in SCLE, owing to basal cell damage in the former and diffuse epidermal damage in the latter.[11]

LTR/IFD has two major component compartments:

  1. Epidermal basal cell layer – focus of injury
  2. Dermal mononuclear inflammatory cell infiltrate – responsible for injury.


In our study, classic lichen planus and lichen striatus had the highest and lowest frequency, respectively, also seen in those of Kumar et al.[13] and Rekha M et al.[14]

The peak age at presentation was 21–40 years, which was similar to that of Chauhan et al.[15] and comparable with that of Maheshwari et al.,[16] though globally the age group of 30–60 years is more common.[16] Males and females were equally affected, in accordance to the global ratio.[17],[18] However, most of the other Indian studies showed female preponderance [13],[14],[16] and few showed male preponderance.[15]

Clinically, most cases of the classic lichen planus were pruritic, violaceous, papules, and plaques involving the limbs, which is the typical presentation.[19] A similar observation has been noted in other studies.[15],[16] Venous stasis has been considered as a factor responsible for this.[20],[21],[22]

About 55.26% of the cases of lichen planus pigmentosus and 50% of ashy dermatosis gave a history of sun exposure, which is thought to be a predisposing factor. The lesions are more common in females and have a predilection for the face and neck.[23] Similar findings were found in our study.

Alopecia is the most common clinical presentation of lichen planopilaris.[11] Fifty percent patients in our study presented with alopecia.

All patients with lichen nitidus had multiple flesh-colored papules involving the limbs and trunk, which is the typical presentation.[10]

Two of three patients with actinic lichen planus had a history of sun exposure and lesions involving the face and neck. Clinically, lichen planus pigmentosus is a close differential diagnosis.[24] Histopathological examination is required to arrive at a definite diagnosis.

As shown in [Table 2], hyperkeratosis and parakeratosis were observed in 80.64% and 12.9% of the cases, respectively, comparable to those of Maheshwari et al.[16] and Chauhan et al.[15] Twenty two cases of lichen planus pigmentosus showed hyperkeratosis, whereas Maheshwari et al.[16] observed the absence of the same.
Table 2: Comparison of histopathologic changes

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Acanthosis was observed in 56.45% of the cases. Its proportion ranged from 55.5% to 83.3% in other studies. About 22.58% of the cases exhibited hypergranulosis. Other studies showed a high variability ranging from 29% to 65.15%, suggesting that acanthosis and hypergranulosis are inconsistent features for diagnosis. Characteristic “claw clutching the ball” appearance was noted in lichen nitidus in ours and other studies.[14]

The hallmark feature of epidermal basal layer injury was the most correlated finding in our study as well as those of Kumar et al.[13] and Chauhan et al.[15] Civatte bodies, though one of the key histologic features of lichenoid IFD, were found to be less correlated in ours (41.93%) and other similar studies.[16]

About 58.06% of our cases showed a band-like mononuclear infiltrate at the dermoepidermal junction, comparable to that of Maheshwari et al.[16]

Lichenoid drug eruptions show numerous eosinophils in the infiltrate.[11] About 62.5% of the cases in our study showed eosinophils.

Caspary Joseph spaces (clefts at the dermoepidermal junction secondary to basal cell damage) were found in a minority of the cases (4.83%) in ours as well as other studies.[15],[16] Up to 17% have been found in other studies.[25]

The most consistent finding in our study was melanin incontinence (90.32% cases), which was similar to that of Kumar et al.[13]

Almost 82.66% of the cases were concordant on histopathology, higher than that of Maheshwari GR et al.'s [16] (78.5%) and Chauhan R et al.'s studies [15] (70.94%).

One case was clinically diagnosed as lichen planus pigmentosus. Histopathology showed spores resembling fungi in the keratin layer, and hence, a diagnosis of dermatophytosis was given.

Another patient presented with multiple hyperpigmented to erythematous macules over the face for 1 year. Lichen planus pigmentosus and ashy dermatosis were the clinical differential diagnoses. However, histopathology showed features of rosacea with Demodex mite in the follicle.

A 17-year-old male patient presented with multiple pruritic hyperpigmented plaques over both the ankles for 10 years. Clinically, hypertrophic lichen planus was suspected. Biopsy revealed marked hyperkeratosis, low papillomatosis with few resembling church spires, and irregular acanthosis of the epidermis. The upper dermis showed moderate perivascular mononuclear inflammatory cell infiltrate with fibrosis. A diagnosis of acrokeratosis verruciformis was suggested.


  Conclusion Top


Familiarity with the characteristics of each LTR/IFD is the key to accomplishing timely recognition and effective management. A lichenoid reaction pattern calls for a set of differential diagnostic considerations. Distinguishing each of these clinically can be challenging. Histopathologic examination of representative skin biopsy serves as a dependable tool for precise diagnosis. Thus, good clinical history, histologic examination, and clinicopathological correlation enable an accurate etiopathologic diagnosis, thereby enhancing patient care.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Pinkus H. Lichenoid tissue reactions. A speculative review of the clinical spectrum of epidermal basal cell damage with special reference to erythema dyschromicum perstans. Arch Dermatol 1973;107:840-6.  Back to cited text no. 1
    
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Hurwitz RM, Rivera HP, Gooch MH, Slama TG, Handt A, Weiss J. Toxic shock syndrome or toxic epidermal necrolysis? Case reports showing clinical similarity and histologic separation. J Am Acad Dermatol 1982;7:246-54.  Back to cited text no. 2
    
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Fitzpatrick JE. New histopathologic findings in drug eruptions. Dermatol Clin 1992;10:19-36.  Back to cited text no. 3
    
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Crowson AN, Magro CM. Idiopathic perniosis and its mimics: A clinical and histological study of 38 cases. Hum Pathol 1997;28:478-84.  Back to cited text no. 4
    
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Iijima W, Ohtani H, Nakayama T, Sugawara Y, Sato E, Nagura H, et al. Infiltrating CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/CXCL10 in their cytolytic granules: A potential self-recruiting mechanism. Am J Pathol 2003;163:261-8.  Back to cited text no. 5
    
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Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: A report of an international consensus meeting: Part1. Viral infections and aetiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:40-51.  Back to cited text no. 6
    
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Shiohara T, Kano Y. Lichen planus and lichenoid dermatoses. In: Bolognia JL, Jorizzo J, Rapini RP, editors. Dermatology. New York, USA: Mosby, Elsevier; 2008. p. 159-80.  Back to cited text no. 7
    
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Shiohara T, Mizukawa Y. The immunological basis of lichenoid tissue reaction. Autoimmun Rev 2005;4:236-41.  Back to cited text no. 8
    
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Sontheimer RD. Lichenoid tissue reaction/interface dermatitis: Clinical and histological perspectives. J Invest Dermatol 2009;129:1088-99.  Back to cited text no. 9
    
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Elder DE, Elenitsas R, Johnson BL, Murphy BF. Introduction to dermatopathologic diagnosis. Lever's Histopathology of the Skin. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 180-214.  Back to cited text no. 10
    
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Patterson JW. Weedon's Skin Pathology. 4th ed. Philadelphia: Churchill Livingstone, Elsevier; 2010. p. 38-152.  Back to cited text no. 11
    
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Breathnach SM. Lichen Planus and Lichenoid Disorders. In: Burns T, Breathnach S, Cox N, Griffiths C (eds). Rook's Textbook of Dermatology. 8th ed. West Sussex, UK: Wiley Blackwell; 2010. p. 41.16.  Back to cited text no. 12
    
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Kumar UM, Yelikar BR, Inamadar AC, Umesh S, Singhal A, Kushtagi AV. A clinico-pathological study of lichenoid tissue reactions-a tertiary care experience. J Clin Diagn Res 2013;7:312-6.  Back to cited text no. 13
    
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Rekha M, Swetha D, Srikanth S. Clinico histological study of Lichenoid dermatoses – A study of one hundread cases. Perspectives Med Res 2015;3:16-20.  Back to cited text no. 14
    
15.
Chauhan R, Srinath MK, Ali NM, Bhat RM, Sukumar D. Clinicopathological study of lichenoid reactions: A retrospective analysis. J Evol Med Dent Sci 2015;4:5551-62.  Back to cited text no. 15
    
16.
Maheshwari GR, Mehta HH, Nikam V. Clinico-histopathological correlation for diagnosis of lichenoid interface dermatoses. J Dermatol Dermatol Surg 2016;20:115-24.  Back to cited text no. 16
    
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Khopkar U, Valia A. Lichen Planus. Vol. 1. Mumbai: Jaypee Brothers Pvt., Ltd.; 2013. p. 1-239.  Back to cited text no. 17
    
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Schmidt H. Frequency, duration and localization of lichen planus. A study based on 181 patients. Acta Derm Venereol 1961;41:164-7.  Back to cited text no. 18
    
19.
Le boit PE. Dermatitis involving dermo-epidermal junction. In: Maize JC, Burgdorf WH, Hurt MA, Le Boit PE, Metcalf JS, Smith T, et al., editors. Cutaneous Pathology. Philadelphia: Churchill Livingstone; 1998. p. 87-145.  Back to cited text no. 19
    
20.
Bhutani LK, Bedi TR, Pandhi RK, Nayak NC. Lichen planus pigmentosus. Dermatologica 1974;149:43-50.  Back to cited text no. 20
    
21.
Black MM. Lichen planus and lichenoid disorders. In: Champion RH, Burton JL, Burns DA, editors. Textbook of Dermatology. 6th ed. Oxford, England: Blackwell Science; 1998. p. 1916-8.  Back to cited text no. 21
    
22.
Scully C, el-Kom M. Lichen planus: Review and update on pathogenesis. J Oral Pathol 1985;14:431-58.  Back to cited text no. 22
    
23.
Ghosh A, Coondoo A. Lichen planus pigmentosus: The controversial consensus. Indian J Dermatol 2016;61:482-6.  Back to cited text no. 23
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24.
Choi K, Kim H, Kim H, Park K. A case of actinic lichen planus. Internet J Dermatol 2009;8:1-5.  Back to cited text no. 24
    
25.
Hegde VK, Khadilkar UN. A clinicopathological study of interface dermatitis. Indian J Pathol Microbiol 2014;57:386-9.  Back to cited text no. 25
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